Abstract

Purpose Pericarditis is a rare finding in primary tuberculosis. Prognosis is excellent with treatment so early diagnosis is crucial. Pathogenesis is particularly important, given that the direct spread from tuberculous pneumonia is uncommon, but instead from mediastinal nodes directly into the pericardium. These mechanisms must be taken in consideration in the interpretation of diagnostic tools.

Case Presentation A 32-year-old female, who moved to Memphis from India 3 years ago, was admitted with a 1-month history of febrile illness, malaise, and weakness; more recently, she also complained of resting dyspnea, which was progressively worsening. A positive PPD and an abnormal chest x-ray prompted hospitalization, where she was found to have pulsus paradoxus of 20 mm Hg. Echocardiogram showed diastolic right chamber collapse along with respiratory variation of the mitral inflow, consistent with pericardial tamponade. A chest CT showed a large pericardial effusion and bilateral pleural effusions. A pericardiocentesis was performed with resolution of her resting dyspnea; 800 cc of serous fluid drained from the pericardial space over the following 24 h. Blood studies were remarkable for an elevated WBC (18,000 cells/μL) with neutrophil predominance. Serum studies showed slight elevation of liver transaminases and significantly elevated CRP (8.1 mg/L) and ESR (98 mm/h); a comprehensive workup for rheumatic diseases revealed no abnormal findings. Sputum and pericardial fluid cultures and smear for AFB and other organisms were negative. Pericardial fluid was exudative LDH 2432 U/L and WBC 10200 cells/μL with neutrophil predominance. Pericardial fluid PCR for M. tuberculosis DNA was negative; adenosine deaminase in pericardial fluid was elevated (44.4 U/L [normals 0-18]). Pericardial biopsy was consistent with chronic pericarditis, but with no evidence of granulomatous disease. The patient was treated with steroids and antituberculous therapy with resolution of the clinical syndrome and no recurrence of the effusion thereafter.

Conclusion Adenosine deaminase, an enzyme marker of cell-mediated immune response activity to M. tuberculosis that includes activated T lymphocytes and macrophages, appears in pericardial fluid. Given the sensitivity and specificity of adenosine deaminase in tuberculous effusions, it is of considerable value in the absence of evidence of infection in the pericardial space. The diagnosis of tuberculous effusion can be made without demonstration of mycobacterium. A high level of suspicion should trigger early aggressive diagnosis with adenosine deaminase and appropriate treatment.

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